ArticleThe Journal of cell biology2025
KPNA3 regulates histone locus body formation by modulating condensation and nuclear import of NPAT.
Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A Simplified Wheat Protoplast Transformation System and Guideline for Avoiding Protein Localization Artifacts.Plants (Basel, Switzerland) · 2026Article
- KAS-CUT&Tag for direct mapping of transcription bubbles.bioRxiv : the preprint server for biology · 2026Article
- From chromosomal protein disorder to chromatin phase separation.Epigenetics & chromatin · 2026Review
- A negative feedback mechanism controls histone gene expression.Nature structural & molecular biology · 2026Article
- Nanobody Nb07 mitigates sepsis by blocking the PFKM-p53-PD-1 axis to enhance macrophage phagocytosis.Theranostics · 2026Article
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13 authors.
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Abstract
The histone locus body (HLB) is a membraneless organelle that determines the transcription of replication-dependent histones. However, the mechanisms underlying the appropriate formation of the HLB in the nucleus but not in the cytoplasm remain unknown. HLB formation is dependent on the scaffold protein NPAT. We identify KPNA3 as a specific importin that drives the nuclear import of NPAT by binding to the nuclear localization signal (NLS) sequence. NPAT undergoes phase separation, which is inhibited by KPNA3-mediated impairment of self-association. In this, a C-terminal self-interaction facilitator (C-SIF) motif, proximal to the NLS, binds the middle 431-1,030 sequence to mediate the self-association of NPAT. Mechanistically, the anchoring of KPNA3 to the NPAT-NLS sterically blocks C-SIF motif-dependent NPAT self-association. This leads to the suppression of aberrant NPAT condensation in the cytoplasm. Collectively, our study reveals a previously unappreciated role of KPNA3 in modulating HLB formation and delineates a steric hindrance mechanism that prevents inappropriate cytoplasmic NPAT condensation.
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